Recent studies have implicated Actinobacillus actinomycetemcomitans as a possible etiologic agent of juvenile periodontitis (periodontosis). The organism has been recovered with greater frequency and in higher numbers from lesions of periodontosis than healthy sites in the same individuals or from lesions of gingivitis or periodontitis (Mandell and Socransky, 1980; Slots et al, 1980). Serum antibody titers to the organism are more frequently elevated in patients with periodontosis, when compared to healty individuals and individuals with other forms of periodontal disease (Ebersole et al, 1980a,b; Genco et al, 1980; Lai and Listgarten, 1980). Strains of Actinobacillus actinomycetemcomitans produce a toxin capable of lysing polymorphonuclear leukocytes (Baehni et al, 1979; Baehni et al, 1980). Antibodies to this toxin may be detected in periodontosis patients which are protective against the toxins lytic effect (McArthur et al, 1980). Actinobacillus actinomycetemcomitans has been shown to accelerate alveolar bone loss in gnotobiotic rats (Irving et al, 1975). Actinobacillus actinomycetemcomitans does not appear to be a numerically dominant member of the microbiota of individuals without adolescent destructive disease, but can attain proportions as high as 70% of the cultivable microbiota in sites of advanced destruction.